the analysis of βcatenin via Wnt signal for adherens system in periodontal tissue

通过Wnt信号分析牙周组织中粘附系统的β连环蛋白

• 批准号: 22792081
• 负责人: SUDA Tomonari
• 金额: $ 2.58万
• 依托单位: Tokyo Medical and Dental University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22792081/
• 关键词: 歯肉上皮細胞; E-cadherin; β-catein; TNFα; β-catenin; 歯肉繊維芽細胞; Wntシグナル; β-integrin

The epithelium provides an important barrier against microbial invasion. Accordingly, the destruction of epithelial barrier caused by inflammatory and microbial stimulation might accelerate the collapse of periodontal tissue. Cadherins play important roles in cell adhesion, ensuring that cells within tissues are bound together. E-cadherins are found in epithelial tissues and key molecule in the formation of adherens junction. E-cadherins suppress Wnt signaling by localizing β-catenin at the site of cell-cell contacts. Integrins mediate the attachment between a cell and extracellular matrix and regulate the location of β-catenin by the suppression of GSK3β, which is mediated via ILK (Integrin-linked kinase). ILK interact with the cytoplasmic domains of the inegrin subunits. The purpose of this study was to examine the effect of Wnt signaling in periodontal tissues on adhesion of cell-cell adhesion and the attachment between a cell and extracellular matrix. Present study showed that Wnt3a stimulation increased β-catenin and decreased β1-integrin. On the contrary, Wnt5a stimulation decreased β-catanin and increased β1-integrin in human gingival fibroblasts. In human gingival epithelial cells, TNFα decreased E-cadherin. The reduction of E-cadherin might be mediated by phosphorylation of β-catenin, which induced the disruption between E-cadherin and β-catenin. In addition, TNFα stimulation caused the translocation of β-catenin from the cell-cell contacts to the nucleus. These results suggest that Wnt signaling affected the adhesion systems in periodontal tissues.

上皮提供了抵抗微生物入侵的重要屏障，因此，炎症和微生物刺激引起的上皮屏障的破坏可能会加速牙周组织的塌陷，从而确保组织内的细胞结合在一起。钙粘蛋白存在于上皮组织中，是形成粘附连接的关键分子，E-钙粘蛋白通过将 β-连环蛋白定位在细胞与细胞接触的部位来抑制 Wnt 信号传导。整合素介导细胞和细胞外基质之间的附着，并通过抑制 GSK3β 来调节 β-连环蛋白的位置，这是通过 ILK（整合素连接激酶）与整合素亚基的细胞质结构域相互作用来介导的。本研究旨在检测牙周组织中Wnt信号传导对细胞间粘附以及细胞与细胞外基质之间附着的影响。本研究表明Wnt3a刺激增加。相反，在人牙龈成纤维细胞中，Wnt5a 刺激会减少 β-catanin 并增加 β1-整合素，而在人牙龈上皮细胞中，TNFα 可能会介导 E-钙粘蛋白的减少。通过 β-连环蛋白的磷酸化，诱导 E-钙粘蛋白和 β-连环蛋白之间的破坏。此外，TNFα 刺激还导致 TNFα 的易位。这些结果表明，Wnt 信号传导影响牙周组织中的粘附系统。